Methylation tolerance in mismatch repair proficient cells with low MSH2 protein level

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Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

To investigate the role of the presumed DNA mismatch repair (MMR) gene Msh2 in genome stability and tumorigenesis, we have generated cells and mice that are deficient for the gene. Msh2-deficient cells have lost mismatch binding and have acquired microsatellite instability, a mutator phenotype, and tolerance to methylating agents. Moreover, in these cells, homologous recombination has lost depe...

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ژورنال

عنوان ژورنال: Oncogene

سال: 2002

ISSN: 0950-9232,1476-5594

DOI: 10.1038/sj.onc.1205395